Transcription factor FOXF2 promotes the development and progression of pancreatic cancer by targeting MSI2.

Pancreatic cancer (PC) is a malignant tumor possessing high mortality. The role of transcription factor Forkhead Box F2 (FOXF2) in PC remains unverified. The current study investigated the roles of FOXF2 in developing PC in vitro and in vivo. A xenograft tumor model was constructed with nude mice injected using FOXF2­overexpressing PC cells or FOXF2­silenced PC cells. High FOXF2 expression significantly enhanced the proliferation ability of PC cells in vitro and pancreatic tumor growth in vivo. The cell cycle analysis indicated that transition of G1­S phase was promoted by FOXF2. The cell cycle­associated proteins cyclin D1, CDK2, phosphorylated (p)­CDK2 and p­RB were upregulated in the FOXF2­overexpressing cells and downregulated in the cells with FOXF2 knockdown. Flow cytometric analysis and Hoechst staining showed that the percentage of apoptotic cells was significantly increased after FOXF2 was silenced. FOXF2 knockdown promoted expression of pro­apoptotic proteins (Bad, Bax and cleaved caspase­3) while suppressing the anti­apoptotic proteins (Bcl­2 and Bcl­xl) at the protein level. FOXF2 improved the migration and invasion of PC cells in vitro. Moreover, luciferase and chromatin immunoprecipitation assays revealed that FOXF2 binds to the MSI2 promoter, promoting its transcriptional expression. FOXF2 knockdown inhibited the MSI2 protein translation while enhancing the translation of NUMB protein, suppressing PC development in vivo. MSI2 silencing reversed the promotive effect mediated by FOXF2 on cell proliferation. These results demonstrated that FOXF2 is essential in PC progression, and the potential mechanism includes regulating MSI2 transcription.

The implication of ciliary signaling pathways for epithelial-mesenchymal transition.

Epithelial-to-mesenchymal transition (EMT), which plays an essential role in development, tissue repair and fibrosis, and cancer progression, is a reversible cellular program that converts epithelial cells to mesenchymal cell states characterized by motility-invasive properties. The mostly signaling pathways that initiated and controlled the EMT program are regulated by a solitary, non-motile organelle named primary cilium. Acting as a signaling nexus, primary cilium dynamically concentrates signaling molecules to respond to extracellular cues. Recent research has provided direct evidence of connection between EMT and primary ciliogenesis in multiple contexts, but the mechanistic understanding of this relationship is complicated and still undergoing. In this review, we describe the current knowledge about the ciliary signaling pathways involved in EMT and list the direct evidence that shows the link between them, trying to figure out the intricate relationship between EMT and primary ciliogenesis, which may aid the future development of primary cilium as a novel therapeutic approach targeted to EMT.

Large left paraduodenal hernia with intestinal ischemia: a case report and literature review.

A left paraduodenal hernia is a rare type of internal hernia but the most common type of peritoneal recess hernia. Preoperative diagnosis of a left paraduodenal hernia is difficult because of its nonspecific clinical manifestations, and it is often confused with other causes of acute abdomen. Diagnosis is therefore often delayed, resulting in serious clinical outcomes. We herein report a case of a large paraduodenal hernia with small intestinal obstruction and ischemia without abdominal pain. The patient was successfully discharged after emergency hernia repair. This case reveals the importance of diagnosing a left paraduodenal hernia with or without abdominal pain, especially in patients with no history of abdominal surgery.

Silencing Formin-like 2 inhibits growth and metastasis of gastric cancer cells through suppressing internalization of integrins.

BACKGROUND: Formin-like 2 (FMNL2) is a member of Formin family which governs cytokinesis, cellular polarity and morphogenesis. Dysregulation of FMNL2 has been discovered in cancers and is closely related to cancers. However, the role of FMNL2 in gastric cancer remains unclear. In this study, we aimed to investigate the role of FMNL2 in gastric cancer cells. METHODS: A FMNL2-specific shRNA was employed to decrease the endogenous expression of FMNL2. Then the degree of proliferation, apoptosis, migration and invasion of gastric cancer cells was assessed by MTT assay, flow cytometry, wound healing assay and transwell assay, respectively. The expression and distribution of FMNL2 and protein kinase C (PKC) α was detected by immunofluorescence. The internalization of integrins was detected by enzyme-linked immunosorbent assay. RESULTS: Our results showed that silencing FMNL2 suppressed proliferation, migration and invasion, and induced apoptosis of gastric cancer cells. The integrin internalization induced by PKC was declined by FMNL2 silencing. CONCLUSIONS: Our study reveals that silencing FMNL2 suppresses growth and metastasis of gastric cancer cells. Modulation on integrin internalization may be implicated in the role of FMNL2 in growth and migration of gastric cancer cells. Our study indicates that FMNL2 may become a potential therapeutic target for gastric cancer.

Solid Pseudopapillary Neoplasm of the Pancreas: Clinicopathologic Feature, Risk Factors of Malignancy, and Survival Analysis of 53 Cases from a Single Center.

INTRODUCTION: Solid pseudopapillary neoplasm (SPN) of the pancreas is a rare tumor of low malignant potential. The aim of this study was designed to evaluate the clinicopathologic feature, predictive factors of malignancy, and survival from experience of a single center. METHODS: 53 consecutive patients who underwent surgery for a pathologically definitive SPN were retrospectively reviewed. RESULTS: A total of 53 cases included 7 male cases and 46 female cases with the median age of 35.4 years (14-67). Abdominal pain and mass were the most common clinical presentations. The radiological presentations were consistent with solid and cystic pattern in 18 cases, solid pattern in 25 cases, and cystic pattern in 10 cases. The predominant location of tumor was pancreatic body and tail. The mean size of the tumors was 6.4 cm. Aggressive en bloc resection combined with organ-preserving should be indicated whenever feasible. Follow-up information was available for 48 patients with a median follow-up time of 48 months. The 5-year disease-specific survival was 95.7%. Incomplete capsule was not only the predictive factor of malignancy but also the significant predictor of disease-specific survival. CONCLUSION: Incomplete capsule may suggest a malignant SPN and a prognostic indicator of disease-specific survival. We recommend that surgeons consider a more radical resection with an incomplete capsule of tumor.

A meta-analysis: could we predict the malignancy of solid pseudopapillary neoplasm?

OBJECTIVE: To evaluate the risk factors influencing the malignant potential of solid pseudopapillary neoplasm (SPN). METHODS: This meta-analysis used MEDLINE (PubMed), EMBASE and web of science including 14 cohort studies reporting the risk factors influencing the malignant potential after the initial operation on SPN up to March 2017. Review Manager Software 5.2 was used for meta-analysis. RESULTS: 14 studies with a total of 763 patients were included in our meta-analysis. In all the variables, age and tumor size were significantly correlated with malignancy. CONCLUSION: Malignant SPNs tended to be larger in diameter and younger in age than benign type. In particularly, larger tumor size may be a crucial factor for decision of aggressive resection.